Format

Send to

Choose Destination
Eur J Gastroenterol Hepatol. 2013 Aug;25(8):953-7. doi: 10.1097/MEG.0b013e32835ed691.

Downregulation of microRNA-206 is a potent prognostic marker for patients with gastric cancer.

Author information

1
Department of Gastroenterology, Tangdu Hospital of Fourth Military Medical University, Xi'an, China.

Abstract

BACKGROUND:

MicroRNA-206 (miR-206), as a homolog of miR-1, plays important roles in tumorigenesis and tumor progression of various human malignancies, including breast cancer, endometrial endometrioid carcinoma, rhabdomyosarcoma, glioma, lung cancer, and laryngeal cancer. However, its involvement in gastric cancer has remained unclear.

AIM:

To examine the expression patterns and clinical implications of miR-206 in gastric cancer.

MATERIALS AND METHODS:

Quantitative RT-PCR was performed to evaluate the expression levels of miR-206 in 98 pairs of gastric cancer and normal adjacent mucosa. In addition, the clinicopathologic significance and the prognostic value of miR-206 expression were further determined.

RESULTS:

At first, miR-206 expression was significantly downregulated in gastric cancer tissues when compared with normal adjacent mucosa (P<0.001). Next, tumors with low miR-206 expression had a greater extent of lymph node metastasis (P=0.01), presence of venous invasion (P=0.008), and hematogenous recurrence (P=0.01), and were at a worse stage (P=0.03) than the tumors with a high miR-206 expression. Then, the gastric cancer patients with a low miR-206 expression had shorter overall survival than those with a high miR-206 expression (P=0.02). Furthermore, multivariate analysis showed that miR-206 expression was an independent prognostic factor for patients with gastric cancer.

CONCLUSION:

Our results strongly suggest that the downregulation of miR-206 was significantly correlated with tumor progression and may be a potent prognostic marker of gastric cancer. miR-206 might serve as a promising therapeutic target for the treatment of this cancer.

PMID:
23751352
DOI:
10.1097/MEG.0b013e32835ed691
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Wolters Kluwer
Loading ...
Support Center